State Key Laboratory of Crop Stress Biology in Arid Areas, College of Horticulture, Northwest A & F University, Yangling 712100, China.
College of Biological and Agricultural Sciences, Honghe University, Mengzi 661100, China.
J Agric Food Chem. 2022 Dec 14;70(49):15401-15414. doi: 10.1021/acs.jafc.2c05998. Epub 2022 Nov 30.
The sex-control system involves several mechanisms in melon. The present study identified a novel bisexual flower control gene from the hermaphroditic melon germplasm, different from the previously recognized one. Genetic analysis showed that a single recessive gene in the newly identified locus controlled the bisexual flower phenotype in melons. We generated 1431 F segregating individuals for genetic mapping of locus , which was delimited to a 47.94 kb region. Six candidate genes were identified in the delimited interval, and candidate No. 4 encoding melon CPR5 protein was selected as the suitable one for locus and was denoted . CPR5 reportedly interacted with ethylene receptor ETR1 to regulate ethylene signal transduction. Moreover, the ethephon assays showed that the parental lines (unisexual line and bisexual line) had contrasting expression patterns of . The BiFC and LCI assays also confirmed that CmCPR5 interacted with CmETR1 in 0426 but not in Y101. However, crossover tests showed that CmETR1 functioned normally in both parental lines, suggesting CPR5 malfunction in Y101. This study proposed a corollary mechanism of bisexual flower regulation during stamen primordium development in which the inhibition of stamen primordia development was prevented by the malfunctioning CmCPR5, resulting in bisexual flowers.
甜瓜的性别控制系统涉及多个机制。本研究从雌雄同株甜瓜种质资源中鉴定出一个新的两性花控制基因,与之前鉴定的不同。遗传分析表明,新鉴定的位点中的单个隐性基因控制甜瓜两性花表型。我们为基因座 生成了 1431 个 F2 分离个体进行遗传作图,该基因座被限定在 47.94 kb 的区域内。在限定的区间内鉴定出 6 个候选基因,候选基因 4 编码甜瓜 CPR5 蛋白,被选为基因座的合适候选基因,并被命名为 。CPR5 据报道与乙烯受体 ETR1 相互作用,以调节乙烯信号转导。此外,乙烯利测定表明,亲本系(单性系和两性系)在 上表现出相反的表达模式。BiFC 和 LCI 测定也证实 CmCPR5 在 0426 中与 CmETR1 相互作用,但在 Y101 中不相互作用。然而,交叉测试表明,CmETR1 在两个亲本系中均正常发挥作用,表明 Y101 中的 CPR5 功能失常。本研究提出了一个在雄蕊原基发育过程中调节两性花的推论机制,其中 CmCPR5 的功能失常阻止了雄蕊原基的发育,导致两性花的产生。